Changes in acid-base status in oxygen toxicity at 230 kPa oxygen as a function of exposure time.

Breathing less than 50 kPa of oxygen over time can lead to pulmonary oxygen toxicity (POT). Vital capacity (VC) as the sole parameter for POT has its limitations. In this study we try to find out the changes of acid-base status in a POT rat model. Fifty male rats were randomly divided into five groups, exposed to 230 kPa oxygen for three, six, nine and 12 hours, respectively. Rats exposed to air were used as controls. After exposure the mortality and behavior of rats were observed. Arterial blood samples were collected for acid-base status detection and wet-dry (W/D) ratios of lung tissues were tested. Results showed that the acid-base status in rats exposed to 230 kPa oxygen presented a dynamic change. The primary status was in the compensatory period when primary respiratory acidosis was mixed with compensated metabolic alkalosis. Then the status changed to decompensated alkalosis and developed to decompensated acidosis in the end. pH, PCO2, HCO3-, TCO2, and BE values had two phases: an increase and a later decrease with increasing oxygen exposure time, while PaO2 and lung W/D ratio showed continuously increasing trends with the extension of oxygen exposure time. Lung W/D ratio was significantly associated with PaO2 (r = 0.6385, p = 0.002), while other parameters did not show a significant correlation. It is concluded that acid-base status in POT rats presents a dynamic change: in the compensatory period first, then turns to decompensated alkalosis and ends up with decompensated acidosis status. Blood gas analysis is a useful method to monitor the development of POT.

Relative roles of intracellular Ca2+ and pH in shaping myocardial contractile response to acute respiratory alkalosis.

During acute respiratory alkalosis, myocardial contractility initially increases but then declines toward control levels. To elucidate the mechanism of this response, two parallel strategies were adopted: isovolumic left ventricular developed pressure (DP) and intracellular pH (pHi) were measured in isolated ferret hearts using 31P-nuclear magnetic resonance spectroscopy, and isometric developed tension (DT) and intracellular Ca2+ concentration ([Ca2+]i) were measured in ferret papillary muscles using microinjected fura 2 salt. When hypocapnia was induced by sudden introduction of perfusate equilibrated with 2% CO2 (from 5% CO2 in control), DP increased to a maximum of 120 +/- 3% (SE; n = 7) of control within 40 s. Afterward, DP decreased toward control levels, reaching a new steady state in 2-3 min. In contrast, pHi increased from control (7.11 +/- 0.01) only after 30 s of hypocapnia and reached a peak of 7.25 +/- 0.02 between 80 and 100 s. Thus pHi lagged behind contractility. In contrast to pHi, [Ca2+]i changed in parallel with DT: when DT reached a maximum (251 +/- 63% of control; n = 5) during hypocapnia, the amplitude of [Ca2+]i transients also peaked (190 +/- 22% of control; n = 5). A simulation of contractile force based on our measurements of pHi and [Ca2+]i, along with published Ca(2+)-tension relations, described adequately the changes in developed force during hypocapnia. These results indicate that the biphasic changes in [Ca2+]i, coupled with an out-of-phase change in pHi, underlie the biphasic response of myocardial contractility to hypocapnia.

The mechanism of hypophosphatemia in acute heat stroke.

Severe heat stroke may be associated with hypophosphatemia and hypocalcemia. Hypophosphatemia is generally observed within hours after onset, but hypocalcemia usually occurs on the second or third day, and after hypophosphatemia has undergone spontaneous correction. A young man displayed respiratory alkalosis during the course of severe heat stroke. The hypophosphatemia abated spontaneously as metabolic acidosis and acute renal failure supervened. Hypocalcemia became prominent and was more severe than that ascribable to uremia. Hypocalcemia was probably the result of calcium phosphate and calcium carbonate deposition in injured skeletal muscle.